There is an entire body of research on the attitudes of A&E nurses towards patients who have taken intentional overdose (McLaughlin, 1994).
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Christopher Littlejohn, PGDip, BSc (nursing), BSc (psychology), RMN, is charge nurse, Tayside Substance Misuse Services, Dundee
This is an aspect of nursing care that brings nurses face to face with moral questions of life and death, confronting them with the limitations of their ability to help someone and can sometimes result in feelings of helplessness. It is perhaps unsurprising then, that many nurses react with anger and frustration and with tactics of avoidance (McLaughlin, 1994).
Why do people take overdoses?
Intentional overdose is usually an attempt to stop suffering, and anyone has the potential to consider it if they perceive their suffering to be intolerable, interminable and inescapable (Chiles and Strosahl, 1995). Those who lack the psychosocial resources that ameliorate suffering are therefore at risk. These resources include:
- Religious beliefs;
- Social support;
- Problem-solving skills.
Psychiatric disorder is a source of suffering that also undermines those important psychosocial resources, and patients with specific psychiatric diagnoses are at increased risk of successfully committing suicide (Box 1). However, the presence of psychiatric disorder does not in itself predict suicidal behaviour, indeed the vast majority of psychiatric patients will never attempt suicide (Mann, 2002). Furthermore, half of intentional overdose cases have no specific psychiatric disorder (Chiles and Strosahl, 1995). Those who are more likely to take an overdose tend to react more pessimistically to stressful events, and usually experience more hopelessness and depression as a result (Mann, 2002).
Chiles and Strosahl (1995) state that their lives are often marked by interpersonal conflict and limited social support, producing:
- Social anxiety;
- Difficulty in forming new relationships.
They often have poor problem-solving skills, coupled with an impatience for results (Chiles and Strosahl, 1995) and are likely to display aggressive and impulsive behavioural traits (Mann, 2002) that are biological as well as psychological. Aggressive and impulsive behaviour is correlated with impaired serotonin functioning in the brain (Gilliam et al, 2000). Childhood adversity, in addition to producing psychological impairment, is suspected of impairing the anatomical development of serotonin systems in the brain (Skodol et al, 2002). This is a possible biopsychosocial mechanism by which people who suffer abuse, neglect and violence in childhood may become self-destructive adolescents and adults. Those born with impaired serotonin systems are more likely to provoke adverse experiences because of their aggressive and impulsive behaviours.
Consistent with this, most patients explain their overdose as a reaction to being in ‘a terrible state of mind’ or ‘an unbearable situation’, feeling a loss of control, wanting to die or wanting to escape from an impossible situation (Schnyder et al, 1999). Patients also commonly describe feelings of despair, emptiness, and anxiety or panic prior to overdosing (Schnyder et al, 1999). Most deny that it was intended to simply ‘manipulate’ others, although some admit wanting people to understand how desperate they were feeling or to seek help from someone or thinking that their death would make things easier for others (Schnyder et al, 1999). Thus, they take intentional overdoses to escape from emotional suffering when they have exhausted all other attempts to cope. Some will be motivated by a serious intent to die, while others will be ambivalent. They may be desperate to find alternative ways of responding to their suffering, yet may die for want of an answer (Chiles and Strosahl, 1995).
The first aim is to ensure the patient’s survival using a logical system of acute assessment and intervention (Clegg and Hope, 1999). Standard resuscitation assessment and interventions should be used (ABC - assess airway, breathing, circulation, and neurological status) (Advanced Life Support Group, 2001). If possible, the amount and type of substance(s) taken, and length of time since ingestion should be ascertained.
Four interventions are traditionally used in treating overdose (Clegg and Hope, 1999):
- Induced vomiting;
- Gastric lavage;
- Whole bowel irrigation;
- Absorbed charcoal.
However, the only routine intervention currently recommended is the use of activated charcoal (Mehta et al, 2004). This is most effective when given within one hour of ingestion. Some poisons are best treated with repeated doses of 50g of activated charcoal every four hours (Mehta et al, 2004) (Box 2, p40). Gastric lavage may be considered in patients who have taken poisons that are not absorbed by activated charcoal - excluding petroleum distillates and corrosives (Box 3, p41). Whole bowel irrigation should only be considered after receiving advice from a national poisons centre (the electronic database can be found on the internet at www.spib.axl.co.uk/toxbase) (Mehta et al, 2004). In severe poisoning haemodialysis or haemoperfusion may be indicated (Boxes 4-5, p42-43).
Antidepressants are commonly prescribed for depression and anxiety disorders (these conditions often coexist). Tricyclics are also prescribed for certain types of neuropathic pain. The majority of deaths occur within six hours of ingestion, and none occur after 24 hours have elapsed (Finnell and Harris, 2000).
Those at greatest risk on presentation are those with (Finnell and Harris, 2000):
- Altered mental status;
- A QRS interval of greater than 0.1 seconds;
- Respiratory depression;
Newer antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), are less cardiotoxic than tricyclics (Mehta et al, 2004). Antidiabetics The main effect of an insulin overdose is prolonged hypoglycaemia, alongside seizures and coma. The depot effect of a large overdose can necessitate continued glucose treatment for up to four days (Spiller, 1998). Surgical excision of the depot site, while not routine, may be considered if the insulin was injected within the past three hours, was a particularly large dose, and was a long-acting preparation (Spiller, 1998).
Hypoglycaemia is increased by the additional ingestion of beta-blockers, alcohol, salicylates, fenfluramine, clofibrate, tetracycline, or monoamine oxidase inhibitors, while hepatic or renal impairment can prolong insulin’s half-life (Spiller, 1998). Prolonged hypoglycaemia can result in cerebral oedema, bradycardia, cardiovascular collapse and hypokalaemia, and if left untreated can lead to permanent neurological damage. Glucagon is likely to be ineffective, as the patient’s hepatic glycogen stores are likely to have been exhausted. Biguanide (metformin) overdose produces initial symptoms of nausea, vomiting and abdominal pain, but hypoglycaemia does not usually occur (Spiller, 1998). More seriously, it induces lactic acidosis, potentially causing confusion, lethargy, coma, seizures, hypotension, tachycardia, ventricular arrhythmias and myocardial infarction (Spiller, 1998).
The development of acidosis can occur a number of hours following ingestion, so observations are required for up to eight hours. Spiller (1998) recommends intubation and artificial hyperventilation to reduce circulating carbon dioxide generated by the acidosis, allowing lactate metabolism to resume. An alternative is to administer insulin intravenously, as it reduces lactate production. The main danger from sulphonylurea overdose is the possibility of prolonged hypoglycaemia (Spiller, 1998). As with insulin overdose, this can lead to either death or permanent neurological damage.
Carbamazepine overdose produces drowsiness or agitation, coma, seizures, hypotension or hypertension, and respiratory depression. Adult respiratory distress syndrome, cardiovascular collapse, cardiac arrhythmias and rhabdomyolysis (reduction in skeletal muscle) are possible. Cardiac and respiratory monitoring should continue for at least 12 hours after ingestion (McCrea, 2002).
Gabapentin overdose produces vomiting, drowsiness, dizziness, ataxia, headache, dilated pupils, faecal incontinence, tachycardia, respiratory depression, hypotension and convulsions. Patients should be observed for four hours following overdose and be given symptomatic and supportive care as required (McCrea, 2002).
Lamotrigine overdose produces nausea, vomiting, drowsiness, diplopia, nystagmus, ataxia, muscle weakness, hypertonia and tremor. It can also produce hypotension, respiratory depression, coma and convulsions. Observations should continue for six hours following overdose and symptomatic and supportive care should be given as required (McCrea, 2002).
Mild phenobarbital overdose can often be characterised by drowsiness, ataxia, slurred speech and hypo-tension. Severe overdose produces coma, respiratory depression, myocardial depression and occasionally cerebral oedema. Observations should continue for at least four hours following overdose (McCrea, 2002).
Phenytoin overdose produces vomiting, ataxia, slurred speech, nystagmus, altered consciousness, confusion and delirium. Occasionally, it can produce severe coma, hypotension and respiratory depression. Observations should continue for at least four hours following overdose, but symptoms can be prolonged, requiring hospitalisation (McCrea, 2002).
A mild overdose of sodium valproate results in gastrointestinal disturbance, drowsiness, dizziness, confusion, ataxia, and irritability. Severe overdose is rare, but produces a sudden deep coma, hypotonia, hyporeflexia, convulsions and respiratory depression. Cerebral oedema can occur up to 72 hours after overdose. Any cardiac effects are usually mild (for example, prolonged QTc interval). Electrolytes and blood gases should be monitored for a minimum of six hours after overdose, and 12 hours for modified-release preparations (McCrea, 2002).
Antipsychotics are usually prescribed for schizophrenia or mania, while smaller doses are prescribed for anxiety. Overdose can produce dystonias (torticollis, or neck twisting; trismus or jaw lock; oculogyric crisis, or locked upward gaze) that respond to diazepam or antimuscarinic drugs. There can also be changes to conscious state and cardiac symptoms. Death following antipsychotic overdose is relatively rare (Pickford, 2000).
If arrhythmias occur, disopyramide, procainamide and quinidine should be avoided as they can have QT-prolonging effects, especially with ziprasidone. In hypotension and circulatory collapse use intravenous fluids and sympathomimetics, with preference for noradrenaline or phenylephrine (Pickford, 2000; Trenton et al, 2003).
Benzodiazepine overdose produces drowsiness, ataxia, slurred speech and coma. Respiratory depression and hypotension are possible, especially when the drugs are combined with alcohol. Patients should be given symptomatic and supportive care as required (McCrea, 2002).
Calcium channel antagonists are prescribed for hypertension and angina. Overdose produces life-threatening hypotension, bradycardia, reduced cardiac output and asystole (Finnell and Harris, 2000). The sudden hypotension can produce shock. There can be confusion, agitation, drowsiness, seizures and hyperglycaemia. The latter is due to decreased insulin production, and can result in ketoacidosis.
Amlodipine has the longest half-life, with a significant overdose producing a toxicity that can last 10 days (Finnell and Harris, 2000). Whole bowel irrigation can be considered following overdose with modified-release preparations. The antidote to calcium channel antagonist overdose is intravenous calcium chloride (Finnell and Harris, 2000) or calcium gluconate (Nelson, 2001). However, digoxin levels should be checked first, as calcium salts can interact with digoxin to produce cardiac arrhythmia. Glucagon can be used to reverse cardiac instability (Finnell and Harris, 2000). Overdose-induced hypotension and bradycardia do not respond to any of the usual treatments.
Dopamine, adrenaline, noradrenaline, dobutamine and isoproterenol are all specifically recommended. Insulin therapy and dextrose infusion can be given for up to four days in the case of unresponsive hypotension. Haemoperfusion may help for refractory hypotension (Finnell and Harris, 2000). Mortality following digoxin overdose is greatest in those with heart disease (Bara, 2001). Early symptoms of overdose include anorexia, nausea, vomiting, headache, lethargy, confusion and visual disturbances (yellow or green halos around lights) (Finnell and Harris, 2000).
Cardiac symptoms - arrhythmias, heart block, ventricular tachycardia, ventricular fibrillation, hypotension and cardiac arrest - can take up to six hours to develop (Finnell and Harris, 2000). The antidote is digoxin-specific Fab antibody fragments (Digibind). Beta blocker overdose should be managed in a similar manner to calcium channel antagonists (Nelson, 2001). Signs of toxicity usually appear within two hours, including seizures, hypotension and bradycardia, which similarly do not respond to usual interventions (Finnell and Harris, 2000). Glucagon-specific receptors on the myocardium are not blocked by beta-antagonists, thus glucagon will increase blood pressure and pulse rate (Finnell and Harris, 2000).
Opioid overdose produces increasing unconsciousness, respiratory depression and pinpoint pupils. Naloxone is an antidote (Mehta et al, 2004), but its relatively short duration of action means the patient can go back into the overdose state as the naloxone is metabolised so repeated doses may be required. With very long-acting opioids, such as methadone and dextropropoxyphene, monitoring may need to be prolonged. Dextropropoxyphene and paracetamol in combination (coproxamol) is the prescription opioid that is responsible for most opioid overdose deaths, and is associated with acute cardiovascular collapse when taken with alcohol (Mehta et al, 2004).
Mild antihistamine overdose produces nausea, vomiting, headache, dilated pupils, dry mouth or skin, urinary retention, flushing, drowsiness, lethargy, ataxia, irritability, agitation, hyperactivity, excitement and tremor. More serious overdoses can produce psychosis, hallucinations, tachycardia, pyrexia, and hypotension or hypertension. Severe overdoses can produce a range of effects, including: respiratory depression or arrest; coma; convulsions; cardiac arrhythmia; rhabdomyolysis (Hartley, 2003).
As little as 10g of paracetamol can produce fatal hepatotoxicity. After overdose there are four recognisable stages (Hamm, 2000). The first covers the initial 24 hours, and the patient experiences anorexia, nausea, vomiting and diaphoresis. Results of biochemical tests are often normal. During the second stage, which occurs between 24 and 72 hours, the patient can become asymptomatic or may experience upper right quadrant pain. In the third stage, occurring between 72 and 96 hours, there is clinical deterioration, with gastrointestinal bleeding, coagulopathy, hypoglycaemia, renal failure and electrolyte imbalance. Death can occur. Beyond this comes the fourth stage (after 96 hours), which is one of recovery.
Antidotes to paracetamol overdose include methionine and acetylcysteine. The latter protects against liver damage if given within eight hours. There have been no deaths among those given acetylcysteine within 16 hours of paracetamol ingestion (Hersh et al, 2000). However, it can also be administered beyond 24 hours to positive effect (Hamm, 2000).
Ingestion of 6-10g of aspirin produces a serious overdose in an adult (Hersh et al, 2000). Initial symptoms include gastrointestinal upset, diaphoresis, fever and tinnitus (with or without hearing loss). Later symptoms include agitation, lethargy, hallucinations, seizures, hyperthermia, metabolic acidosis and clotting inhibition. Sodium bicarbonate increases urinary excretion and haemodialysis is indicated in serious cases (Muller, 2003).
Ibuprofen has a relatively low toxicity, even in overdose. The main symptoms are gastrointestinal disturbances (nausea, vomiting, abdominal and epigastric pain) and tinnitus. Symptoms usually arise within four hours of ingestion. Haematemesis, drowsiness, ataxia, dizziness, headache, nystagmus, hypotension, hypokalaemia or hyperkalaemia, convulsions, coma and apnoea can occasionally occur (Hartley, 2003; Hersh et al, 2000).
Cocaine overdose produces hypertension and tachycardia with concurrent constriction of the coronary vessels. The reduction in blood supply in the presence of increased demand leads to myocardial ischaemia, myocardial infarct, cardiac dysrythmia and acute pulmonary oedema (Finnell and Harris, 2000). Administering benzodiazepines decreases the sympathomimetic action of cocaine. However in unresponsive hypertension nitroprusside or phentolamine can be used. For cocaine-induced chest pain, the patient should be oxygenated and given aspirin and diazepam, and sublingual nitroglycerine can be used for unresponsive pain. For benzodiazepine-resistant supraventricular tachycardia, adenosine and labetalol can be used. Note that using lidocaine for ventricular dysrythmias can worsen cocaine toxicity (Finnell and Harris, 2000).
Amphetamine overdose can result in cardiac dysrythmias, tachycardia, hypertension, angina, acute myocardial infarction, congestive heart failure, seizures, hyperthermia and intracranial haemorrhage. There can be later complications including rhabdomyolysis, renal failure and disseminated intravascular coagulation (Finnell and Harris, 2000).
The initial symptoms of theophylline overdose include nausea, vomiting, abdominal pain, haematemesis, diarrhoea, ataxia, agitation, tremor, hyperventilation and tachycardia (Colbridge, 2001). Occasionally there can be hallucinations and electrolyte imbalances. In severe cases there can be hypotension, convulsions, dysrythmias and cardiac arrest. Most theophylline preparations are modified release, so the effects of an overdose can be delayed for up to 24 hours. It should be noted that in vomiting patients it is safe to give ranitidine for excess acid, but not cimetidine as it increases theophylline’s half-life by 60 per cent (Colbridge, 2001).
Meeting the physical needs is only one part of the nursing care required for cases of intentional overdose, as these patients are psychologically vulnerable. Common feelings that overdose survivors experience are shame, guilt and feeling ‘exposed’, with a desire to remain invisible to the health care workers around them (Wiklander et al, 2003). A patient’s lack of communication is an obvious response to these feelings. The most immediate helpful nursing response is therefore to interact with the patient in a kind, caring and respectful way (Wiklander et al, 2003). It is important not to get anxious at not knowing the solution to the patient’s problems. Do not moralise, and do not coerce or threaten with dire consequences should they do this again (Chiles and Strosahl, 1995). While not condoning the patient’s behaviour, the most helpful attitude to adopt is one of understanding that human suffering sometimes results in drastic and mistaken responses. This attitude is most evident in a willingness to actively listen to the patient, and to express empathy for their experience (Schnyder et al, 1999).
Clearly, the psychological traumas that patients have to live with are not going to be resolved in A&E. Since psychotherapy can help reduce repeated suicidal behaviour (Salkovskis et al, 1990), follow-up counselling or mental health intervention can be a vital determinant in the patient’s future outcome. However, mental health resources for such patients can be lacking (Kerkhof, 1994) and patients can be resistant to help even when it is available (Wiklander et al, 2003). Given what we know about patients’ predispositions towards intentional overdose behaviour, it is not surprising that many go on to repeat the behaviour, with fatal consequences.
In one study 12 per cent of intentional overdose patients repeated their overdose, almost half of these took place within three months (Boyes, 1994). Others found that one-quarter of suicidal adolescent patients repeated their suicide attempt within a year (Hulten et al, 2001).
There are two specific brief psychological interventions that can be useful in caring for intentional overdose cases:
- Solution-focused therapy (SFT) takes a future-oriented stance to identify immediate mechanisms for change (Sharry et al, 2002);
- Motivational interviewing (MI) (Miller and Rollnick, 2002) has also been developed to help clinicians address a range of health-related behaviours (Rollnick et al, 1999).
One A&E psychiatric liaison team treated 40 intentional overdose patients with SFT, of whom only one repeated the overdose behaviour within six months (Wiseman, 2003). According to Sharry et al (2002), SFT:
- Highlights patients’ strengths rather than weaknesses;
- Focuses upon exceptions to the problem rather than the problem itself;
- Seeks out solutions and practical goal-setting by using scaling questions and visualising success.
SFT is a collaborative intervention that facilitates patients’ own problem-solving and is intentionally brief in application. Although SFT and MI were developed independently, the similarities in their approach have not gone unnoticed (Lewis and Osborn, 2004). MI is a patient-centred counselling approach, directed at resolving the ambivalence thought to lie at the heart of behaviour change. By engaging the patient in a discussion of both the perceived benefits and costs of a particular behaviour, the aim is to increase the discrepancy between the patient’s values, ambitions and ideal behaviour, and their actual current behaviour. By avoiding an emotional and/or moralistic interaction with the patient, the nurse can treat overdose behaviour as a ‘matter-of-fact’ response to emotional suffering, explore the perceived benefits of this to the patient, and also the less positive consequences. This opens up the opportunity to discuss alternative coping responses, and how one might go about learning them.
Intentional overdose behaviour can lead to a fatal patient outcome and is best understood from a biopsychosocial perspective. Its nature can provoke a range of distressing reactions in nurses. However, the acute nurse who is supported and supervised and can develop a realistic awareness and acceptance of their human abilities, limitations and responsibilities can provide a range of therapeutic nursing interventions that address patients’ physical and psychosocial needs. This article has been double-blind peer-reviewed.